Hotline:400-820-3792Inhibitors?ScreeningLibraries?Proteinswww.MedChemEKY19334Cat.No.:HY-178227CASNo.:2319609-67-9分?式:C??H??N?O?分?量:307.3作?靶點(diǎn):Wnt;β-catenin;CDK作?通路:StemCell/Wnt;CellCycle/DNADamage儲(chǔ)存?式:PleasestoretheproductundertherecommendedconditionsintheCertificateofAnalysis.BIOLOGICALACTIVITY?物活性KY19334?種CXXC5-DVL抑制劑。KY19334可通過(guò)抑制CXXC5-Dvl的相互作?來(lái)激活Wnt/β-連環(huán)蛋?通路。KY19334可通過(guò)抑制CDK1來(lái)抑制癌細(xì)胞的增殖、遷移、侵襲和轉(zhuǎn)化。KY19334能夠加速傷?愈合并發(fā)揮再?作?。KY19334可?于癌癥、炎癥、神經(jīng)系統(tǒng)和代謝性疾病的研究，如?膚鱗狀細(xì)胞癌和糖尿病[1]。IC50&TargetCDK1體外研究KY19334(5μM,72h)inhibitstheproliferationofhumancutaneoussquamouscellcarcinoma(cSCC)cellsHSC-1andHSC-5,butexertsnosignificantproliferationinhibitiononnormalkeratinocyteHaCaTcells[1].KY19334(5μM,24h)significantlyinhibitsthemigrationandinvasionofHSC-1andHSC-5cells[1].KY19334(5μM,2weeks)inhibitsthecolonyformationofHSC-1andHSC-5cells[1].KY19334(5μM,24h)downregulatesCDK1expressionandinhibitstheWnt/β-cateninsignalingpathwayinHSC-1andHSC-5cells[1].KY19334(1mM,7-16days)activatestheWnt/β-cateninsignalingpathwayinkeratinocytes,vascularendothelialcells,andfibroblastsofwoundtissuesfromdiabeticmice[2].KY19334(1mM,7days)promotestheexpressionofangiogenesis-relatedproteinsinCD31+vascularendothelialcellsofdiabeticmousewoundtissues[2].WesternBlotAnalysis[1]CellLine:HSC-1andHSC-5cellsConcentration:5μMIncubationTime:24h1/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemEResult:ReducedCDK1levelsbyapproximately50%.DidnotaltertheexpressionofCDK4.Increasedthephosphorylationofβ-cateninatSer33/37/Thr41.Downregulatedtheexpressionofdownstreamtargetgenesc-MycandCyclinD1.ELISAAssay[2]CellLine:CD31+vascularendothelialcellsofdiabeticmousewoundtissuesConcentration:1mMIncubationTime:7daysResult:IncreasedVEGFAsecretion(approximately80%),CD31+capillarydensity(approximately75%)andVEGFR2proteinlevel(approximately65%).Downregulatedtheexpressionofanti-angiogenicfactorSerpinF1(PEDF)(approximately50%).體內(nèi)研究KY19334(2mM,topicallyapplication,30minsbeforeeachTPA)significantlyinhibitsthedevelopmentofDMBA(HY-W011845)/TPA-inducedskincancerinC57BL/6mice[1].KY19334(1mM,topicallyapplication,dailyfor16days)accelerateswoundhealingindiabeticC57BL/6mice[2].AnimalModel:DMBA(HY-W011845)/TPA-inducedskincancerC57BL/6micemodels[1]Dosage:2mMAdministration:Topicallyapplication,30minsbeforeeachTPAResult:Decreasedtumornumbersandaveragesize.Improvedtumorgrading.Reducedtheproportionsofhyperplasia,papillomaandcarcinomainsitu.DecreasedtheproportionofSCC.DownregulatedtheexpressionsofCDK1,β-catenin,c-Myc,CyclinD1andPCNAintumortissues.Upregulatedtheexpressionsoftumorsuppressorproteinsp21Cip/WAFandp27.AnimalModel:HFD(highfatdiet)+STZ(HY-13753)-induceddiabeticC57BL/6miceanddb/dbmice[2]Dosage:1mMAdministration:Topicallyapplication,dailyfor16daysResult:Increasedthewoundclosurerate.Enhancedcollagendepositioninwoundtissues.2/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemERestoredtheproliferationofKeratin14+keratinocytesandCD31+capillarydensity.Increasednuclearβ-cateninexpression.REFERENCES[1].LeeSH,etal.NovelsmallmoleculesdownregulateCDK1expressionandinhibitWnt/β-cateninsignalingincutaneoussquamouscellcarcinomabytargetingitsdistincttumor-specificcellularlandscape.ExpMolMed.2025Sep;57(9):1996-2009.[2].KimE,etal.InhibitingthecytosolicfunctionofCXXC5acceleratesdiabeticwoundhealingbyenhancingangiogenesisandskinrepair.ExpMolMed.2023Aug;55(8):1770-1782.McePdfHeightCaution:P